Cirrhotic ascites review: Pathophysiology, diagnosis and management

Ascites is a pathologic accumulation of peritoneal fluidcommonly observed in decompensated cirrhotic states. Its causes are multi-factorial, but principally involve significant volume and hormonal dysregulation in the setting of portal hypertension. The diagnosis of ascites is considered in cirrhotic patients given a constellation of clinical and laboratory findings, and ultimately confirmed, with insight into etiology, by imaging and paracentesis procedures. Treatment for ascites is multimodal including dietary sodium restriction, pharmacologic therapies, diagnostic and therapeutic paracentesis, and in certain cases transjugular intra-hepatic portosystemic shunt. Ascites is associated with numerous complications including spontaneous bacterial peritonitis, hepato-hydrothorax and hepatorenal syndrome. Given the complex nature of ascites and associatedcomplications, it is not surprising that it heralds increased morbidity and mortality in cirrhotic patients and increased cost-utilization upon the health-care system. This review will detail the pathophysiology of cirrhotic ascites, common complications derived from it, and pertinent treatment modalities.

Procalcitonin,and cytokines document a dynamic inflammatory state in non-infected cirrhotic patients with ascites

AIM:To quantitate the simultaneous serum and ascitic fluid levels of procalcitonin and inflammatory markers in cirrhotics with and without ascites.METHODS:A total of 88 consecutive severe cirrhotic patients seen in a large city hospital liver clinic were studied and divided into two groups,those with and without ascites.Group 1 consisted of 41 cirrhotic patients with massive ascites,as demonstrated by necessity for therapeutic large-volume paracentesis.Group 2consisted of 47 cirrhotic patients without any clinically documented ascites to include either a recent abdominal computed tomography scan or ultrasound study.Serum and ascitic fluid levels of an array of inflammatory markers,including procalcitonin,were measured and compared to each other and a normal plasma panel(NPP).RESULTS:The values for inflammatory markers assayed in the serum of Groups 1 and 2,and ascitic fluid of the Group 1.The plasma levels of the inflammatory cytokines interleukin(IL)-2,IL-4,IL-6,IL-8,interferon gamma(IFNγ)and epidermal growth factor(EGF)were all significantly greater in the serum of Group 1as compared to that of the serum obtained from the Group 2 subjects(all P<0.05).There were significantly greater serum levels of IL-6,IL-8,IL-10,monocyte chemoattractant protein-1,tumor necrosis factor-α,vascular endothelial growth factor and EGF when comparing Group 2 to the NPP.There was no significant difference for IL-1A,IL-1B,IL-2,IL-4 and IFNγlevels between these two groups.Serum procalcitonin levels were increased in cirrhotics with ascites compared to cirrhotics without ascites,but serum levels were similar to ascites levels within the ascites group.Furthermore,many of these cytokines,but not procalcitonin,demonstrate an ascites-to-serum gradient.Serum procalcitonin does not demonstrate any significant difference segregated by liver etiology in the ascites group;but ascitic fluid procalcitonin is elevated significantly in car-diac cirrhosis/miscellaneous subgroup compared to the hepatitis C virus and alcoholic cirrhosis subgroups.CONCLUSION:Procalcitonin in the ascitic fluid,but not in the serum,differentiates between cirrhotic subgroup reflecting the dynamic interplay of ascites,bacterial translocation and the peri-peritoneal cytokine.